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在颞叶癫痫大鼠模型中miR-146a/补体因子H介导的炎症反应的调节

Modulation of miR-146a/complement factor H-mediated inflammatory responses in a rat model of temporal lobe epilepsy.

作者信息

He Fang, Liu Bei, Meng Qiang, Sun Yang, Wang Weiwen, Wang Chao

机构信息

Outpatient Department, The 316 Military Hospital, Beijing 100093, China.

Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, China.

出版信息

Biosci Rep. 2016 Dec 23;36(6). doi: 10.1042/BSR20160290. Print 2016 Dec.

DOI:10.1042/BSR20160290
PMID:27852797
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5180253/
Abstract

Increasing evidence supports the involvement of inflammatory and immune processes in temporal lobe epilepsy (TLE). miRNAs represent small regulatory RNA molecules that have been shown to act as negative regulators of gene expression controlling different biological processes, including immune system homoeostasis and function. We investigated the expression and cellular distribution of miRNA-146a (miR-146a) in a rat model of TLE. Prominent up-regulation of miR-146a activation was evident in 1 week after status epilepticus (SE) and persisted in the chronic phase. The predicted miR-146a's target complement factor H (CFH) mRNA and protein expression was also down-regulated in TLE rat model. Furthermore, transfection of miR-146a mimics in neuronal and glial cells down-regulated CFH mRNA and protein levels respectively. Luciferase reporter assays demonstrated that miR-146a down-regulated CFH mRNA expression via 3'-UTR pairing. Down-regulating miR-146a by intracerebroventricular injection of antagomir-146a enhanced the hippocampal expression of CFH in TLE model and decreased seizure susceptibility. These findings suggest that immunopathological deficits associated with TLE can in part be explained by a generalized miR-146a-mediated down-regulation of CFH that may contribute to epileptogenesis in a rat model of TLE.

摘要

越来越多的证据支持炎症和免疫过程参与颞叶癫痫（TLE）。微小RNA（miRNA）是一类小的调节RNA分子，已被证明可作为基因表达的负调节因子，控制包括免疫系统稳态和功能在内的不同生物学过程。我们研究了miRNA-146a（miR-146a）在TLE大鼠模型中的表达及细胞分布。癫痫持续状态（SE）后1周，miR-146a激活明显上调，并在慢性期持续存在。在TLE大鼠模型中，预测的miR-146a靶标补体因子H（CFH）的mRNA和蛋白表达也下调。此外，在神经元和神经胶质细胞中转染miR-146a模拟物分别下调了CFH的mRNA和蛋白水平。荧光素酶报告基因检测表明，miR-146a通过3'-UTR配对下调CFH mRNA表达。通过脑室内注射抗miR-146a下调miR-146a可增强TLE模型中海马CFH的表达，并降低癫痫易感性。这些发现表明，与TLE相关的免疫病理缺陷部分可由miR-146a介导的CFH普遍下调来解释，这可能在TLE大鼠模型的癫痫发生中起作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/0a7d24bfbe91/bsr036e433fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/3c2397c0958b/bsr036e433fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/8290ac2b9d23/bsr036e433fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/9e3ee862bf3b/bsr036e433fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/0575ed54dd57/bsr036e433fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/5522205bc990/bsr036e433fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/0a7d24bfbe91/bsr036e433fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/3c2397c0958b/bsr036e433fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/8290ac2b9d23/bsr036e433fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/9e3ee862bf3b/bsr036e433fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/0575ed54dd57/bsr036e433fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/5522205bc990/bsr036e433fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f88/5180253/0a7d24bfbe91/bsr036e433fig6.jpg

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